The JI
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     
 

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Leibnitz, R. R.
Right arrow Articles by Thiele, D. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Leibnitz, R. R.
Right arrow Articles by Thiele, D. L.

The Journal of Immunology, Vol 155, Issue 4 1784-1795, Copyright © 1995 by American Association of Immunologists

ARTICLES

Protection from T helper cell-mediated graft-versus-host disease by the presence of an MHC class I alloantigen is associated with perturbation of MHC class II-restricted responses by class I-derived peptides

RR Leibnitz, PE Lipsky and DL Thiele
Immunology Graduate Program, University of Texas Southwestern Medical Center at Dallas 75235, USA.

Lethal graft-vs-host disease (GVHD) develops after transfer of CTL- depleted spleen and bone marrow cells from C57BL/6 (B6) mice to irradiated MHC class II disparate (B6xbm12)F1 recipients. Onset of lethal GVHD is significantly delayed in (bm1xbm12)F1 recipients of the same donor inoculum despite the additional MHC class I disparity (H- 2Kbm1). To investigate the basis of this protective effect, hybridomas were generated from T cells activated in vivo during GVHD in both strain combinations. T cells from B6-->(B6xbm12)F1 mice generated a significantly higher frequency of B6.C-H-2bm12 (bm12)-specific T hybridomas (110/178, 62%) than T cells from B6-->(bm1xbm12)F1 mice (102/218, 47%). Some bm12-specific T hydridomas exhibited lesser responses to (bm1xbm12)F1 than to (B6xbm12)F1 APC. Moreover, bm1 peptides spanning a 14-amino acid region that includes the three amino acids that differ from H-2Kb were found to inhibit responses of some bm12-specific T hybridomas and to decrease significantly responses of splenic B6 CD4+ T cells to bm12 APC. Notably, the frequency of bm12- reactive hybridomas susceptible to inhibition by bm1 peptides generated from B6-->(B6xbm12)F1 mice was significantly greater than that generated from B6-->(bm1xbm12)F1 mice. Additional analysis using L cell transfectants indicated that hybridomas responding to the bm12 mutation at position 70 alone were rarely inhibited by bm1 peptides. The data indicate that expression of bm1-derived peptides can influence the frequency and specificity of alloreactive CD4+ T cells stimulated in vivo and thus may alter the course of GVHD.




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 1995 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 1995 by The American Association of Immunologists, Inc. All rights reserved.